Nervous system 1 Introduction, raised intracranial pressure and trauma Professor John Simpson

Nervous system 1Introduction, raised intracranial

pressure and traumaProfessor John Simpson

This lecture will cover

• NS cell reactions to injury

• raised intracranial pressure, including herniation of the brain

• traumatic brain injury

What’s different about the nervous system to all other body systems?

Why is the NS different?

• brain and cord sit in closed spaces• autoregulation of blood flow• blood-brain barrier• high dependency on O2 and glucose• absence of lymphatics• limited immune surveillance• unique cell population with distinctive

responses to injury and healing

Microscopic structure of the nervous system

• neurons (essentially end cells)– cell bodies - aggregated in grey matter

• layers, ganglia, columns, nuclei• In specific domains

– cell processes - include• axons in bundles in white matter

• glial cells (capable of dividing)– astrocytes, oligodendrocytes and ependyma –

neuroectodermal origin– microglia – mesodermal origin

Glial cell roles

• astrocytes– neuronal support, blood-brain barrier, healing and

repair (by gliosis)

• oligodendrocytes– myelin production (~ = Schwann cells in periphery)

• ependyma– related to choroid plexus/CSF production

• microglia– NS macrophages

Cellular reaction to injury - neurons

• cell death– in chronic disease, often seen as reduced

cellularity

• cell “degeneration”– variety of changes ~ disease, e.g.

accumulations, inclusions

• axonal reaction– regeneration possible if only axon damaged

How might diseases of the nervous present?

Symptoms and signs of NS disease

• headache• neck stiffness• coma/impaired consciousness• loss or disturbance of movement• abnormal reflexes• muscle atrophy• sensory impairment/paraesthesia• visual disturbances• tinnitus/deafness

Intracranial pressure (ICP)

• major components of ICP– brain, CSF and blood

• increased volume of any one will raise ICP, unless compensatory reduction in one/both of other components

• presence of anything else “extra” inside skull will do the same

• if ICP continues to increase, compensatory mechanisms will fail

Common causes of raised ICP• intracranial expanding lesions (“space-

occupying lesions”) – e.g. tumour, haematoma, abscess

• hydrocephalus (excess CSF)• cerebral oedema – increase in brain water

content, due to blood-brain barrier problem– localised (e.g. around tumours)– generalised (e.g. following severe head injury or

hypoxic brain damage)

Possible effects of raised ICP

• compression of veins and ventricles• reduced CSF• flattening of gyri and narrowing of sulci• papilloedema• midline shift• herniation of parts of brain• eventual compression of vital brain stem centres• (before skull sutures fused, enlarged cranium)

Raised intracranial pressureRaised intracranial pressure

Decompensation- causes “shifts” and herniation

Cushing reflex- haemodynamic changes (raised BP, slowed pulse)

Focal cerebral oedema infrontal lobe

Focal cerebral oedema in frontal lobe around metastaticcarcinoma

Sites of brain herniation

• subfalcine

• (trans)tentorial

• tonsillar

• (also through skull defect in trauma)

Herniation of the brain

Subfalcine herniation

• (= supracallosal or cingulate hernia)• usually due to primary abnormality in one

cerebral hemisphere• ipsilateral cingulate gyrus herniates under

the free edge of falx• pericallosal arteries are compressed, so

possible cerebral infarction• anterior cerebral artery may also be

affected, causing larger infarct

Subfalcine herniadue to glioblastoma

Tentorial herniation • medial aspect of temporal lobe through

tentorium– affects hippocampus

• midbrain compressed and distorted– compressed aqueduct impairs CSF flow

(obstructive hydrocephalus)– haemorrhage in pons and midbrain

• risk to – ipsilateral 3rd nerve– posterior cerebral artery– opposite cerebral peduncle

Tentorial herniation

Large tentorial hernia due to cerebral glioblastoma

Brain herniation

Figure 28-3 Duret hemorrhage involving the brainstem at the junction of the pons and midbrain.

Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 2 February 2007 01:43 PM)

© 2005 Elsevier

Pontine haemorrhages after tentorial herniation

Central brainstem haemorrhage and necrosis following tentorial herniation

Tonsillar herniation

• (= foramen magnum or foraminal herniation = coning)

• cerebellar tonsils move down – with medulla form “cone” shape

• exit from 4th ventricle blocked impairing CSF flow (obstructive hydrocephalus)

• compression of breathing and cardiac centres in medulla

Tonsillar herniation

Cerebellar tonsillar necrosisfollowing tonsillarherniation

Lumbar puncture

Lumbar puncture is dangerous and should be avoided if ICP raised. Why?

Is there any way you might check for raised ICP before doing an LP?

Traumatic brain injury

• missile or non-missile - latter commoner• in non-missile, primary or secondary damage

– primary – focal lesions (contusion/tear) or diffuse axonal injury

– secondary – e.g. traumatic vascular injury with intracranial haematoma, oedema, herniation, infarction, hydrocephalus, infection

• clinical effects– minor (?) - concussion – major – e.g. death, epilepsy, persistent vegetative

state (PVS), post traumatic dementia

Brain – tearing missile injury

Cerebral contusions

• coup – immediately under site of injury

• contre coup– at opposite side of brain

Frontal, temporal and cerebellar contusions

Temporal lobe contusions

Coup and contre coup

Diffuse axonal injury

• particularly in deep white matter

• even with very minor trauma

• axonal swelling and focal haemorrhage

• contribute to cerebral oedema and raised ICP

• long term effects variable

Traumatic vascular injury

• extradural– especially injury to middle meningeal artery– classical clinical presentation

• subdural– dural veins, ? shearing stress– acute or chronic (? recurrent bleeding)– more common in the elderly and in any bleeding

diathesis– injury often trivial /missed

• (subarachnoid and intracerebral– usually secondary to contusions)

Skull fracture

Extradural v subdural haematoma

Extradural haematoma & multiple contusions

Extradural haemorrhage

Subdural haematoma

Subdural haematoma

Spinal cord trauma

• most often due to accidents and displacement of vertebral column +/- vascular problem

• cord/nerve root compression, transection etc

• effects depend on site and severity– paraplegia, quadriplegia, respiratory

compromise